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缺血再灌注期间离体兔心脏肌膜和线粒体的超微结构变化

Ultrastructural changes of sarcolemma and mitochondria in the isolated rabbit heart during ischemia and reperfusion.

作者信息

Post J A, Leunissen-Bijvelt J, Ruigrok T J, Verkleij A J

出版信息

Biochim Biophys Acta. 1985 Apr 22;845(1):119-23. doi: 10.1016/0167-4889(85)90062-x.

DOI:10.1016/0167-4889(85)90062-x
PMID:3978125
Abstract

Isolated rabbit hearts were perfused by the Langendorff technique, made ischemic and subsequently reperfused. It was found that ischemia results in: (i) aggregation of the intramembranous particles in the sarcolemma and (ii) extrusion of pure lipidic multilamellar structures (liposomes) from swollen mitochondria. Subsequent reperfusion resulted in further aggregation of the sarcolemmal intramembranous particles and disruption of the sarcolemma, which was attended by the formation of liposome-like structures. Intramembrane particle aggregation is explained in terms of lateral phase separation of the membrane lipids and a reduction of repulsive forces between the membrane proteins, both induced by a decrease in pH and an increase in Ca2+ concentration intracellularly. The formation and extrusion of the multilamellar structures are discussed in terms of destabilization of the bilayer which results in a structural blebbing-off of pure lipid.

摘要

采用Langendorff技术对离体兔心进行灌注,使其缺血,随后再灌注。结果发现,缺血导致:(i)肌膜内的膜内颗粒聚集;(ii)肿胀的线粒体挤出纯脂质多层结构(脂质体)。随后的再灌注导致肌膜内的膜内颗粒进一步聚集以及肌膜破裂,并伴有脂质体样结构的形成。膜内颗粒聚集可通过膜脂质的侧向相分离以及膜蛋白之间排斥力的降低来解释,这两者均由细胞内pH值降低和Ca2+浓度升高所诱导。多层结构的形成和挤出则是根据双层结构的不稳定来讨论的,这种不稳定导致了纯脂质的结构泡状脱离。

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